@article{ae647a47c3e3417595771b6361b72f65,
title = "Fibroblast growth factor-2 inhibits CD40-mediated periodontal inflammation",
abstract = "Fibroblast growth factor-2 (FGF-2) stimulates periodontal regeneration by a broad spectrum of effects on periodontal ligament (PDL) cells, such as proliferation, migration, and production of extracellular matrix. A critical factor in the success of periodontal regeneration is the rapid resolution of inflammatory responses in the tissue. We explored an anti-inflammatory effect of FGF-2 during periodontal regeneration and healing. We found that FGF-2 on mouse periodontal ligament cells (MPDL22) markedly downregulated CD40 expression, a key player of inflammation. In addition, FGF-2 inhibited CD40 signaling by the non-canonical nuclear factor-kappa B2 (NFκB2) pathway, resulting in decreased production of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), which have the potential to recruit immune cells to inflamed sites. Furthermore, in vivo treatment of FGF-2 enhanced healing of skin wounds by counteracting the CD40-mediated inflammation. These results reveal that FGF-2 has an important function as a negative regulator of inflammation during periodontal regeneration and healing.",
keywords = "CD40, anti-inflammation, fibroblast growth factor-2 (FGF-2), periodontal ligament (PDL) cells, wound healing",
author = "Chiharu Fujihara and Yu Kanai and Risa Masumoto and Jirouta Kitagaki and Masahiro Matsumoto and Satoru Yamada and Tetsuhiro Kajikawa and Shinya Murakami",
note = "Funding Information: Special funds for the Challenge to Intractable Oral Diseases in Osaka University; Institutional research grant funding from Kaken Pharmaceutical Co., Ltd.; Grants‐in‐Aid for Scientific Research from the Japanese Society for the Promotion of Science, Grant/ Award Numbers: 15H06391, 17K17349; Special funds for the young investigators in Osaka University Funding Information: We appreciate Kaken Pharmaceutical Co., Ltd. for the technical support. This work was supported by Grants-in-Aid for Scientific Research from the Japanese Society for the Promotion of Science (No. 15H06391 and No. 17K17349 to C. Fujihara), special funds for the Challenge to Intractable Oral Diseases and the young investigators in Osaka University, and institutional research grant funding to S. Murakami from Kaken Pharmaceutical Co., Ltd. All authors approved the current and any revised version to be submitted. Funding Information: We appreciate Kaken Pharmaceutical Co., Ltd. for the technical support. This work was supported by Grants‐in‐Aid for Scientific Research from the Japanese Society for the Promotion of Science (No. 15H06391 and No. 17K17349 to C. Fujihara), special funds for the Challenge to Intractable Oral Diseases and the young investigators in Osaka University, and institutional research grant funding to S. Murakami from Kaken Pharmaceutical Co., Ltd. All authors approved the current and any revised version to be submitted.",
year = "2019",
month = may,
doi = "10.1002/jcp.27469",
language = "English",
volume = "234",
pages = "7149--7160",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley-Liss Inc.",
number = "5",
}